The basic hypothesis proposed here is that in hypertrophied myocardium secondary to pressure overload there is a slower than normal rate of crossbridge detachment from actin active sites. Consequently active tension levels are relatively normal whereas the rate of tension development and shortening are slower than normal. Based on the above, and the increase above normal in the number of series and parallel sarcomeres, active muscle stiffness measured with rapid sarcomere length transients should be greater than normal in hypertrophy during tension development and shortening. Furthermore tension redevelopment after a sarcomere length transient should be slower than normal. Tetanized cardiac muslce (high calcium and caffeine) will be used to attain a high, stable activation level. Sarcomere length measured from diffraction of a laser beam by the muscle and a servo-controlled motor will be combined to produce sarcomere length controlled rapid length perturbations and rapid force transients with sarcomere length measurements. The distribution of sarcomere lengths within the areas sampled by the laser will be quantitated with photomicrography. The goal of these experiments is a comparison of normal with hypertrophied myocardium at the sarcomere level and with measures that are referrable to crossbridge populations and kinetics.